Gestational diabetes (hyperglycaemia) is an elevated blood sugar level diagnosed during the period of pregnancy and affects the baby's health. Hyperglycaemia has been found within the gestational weeks between 24 and 28, and the foetus has also the possibility of getting out prior to this test frame; it causes excessive birth weight, early birth, low-blood sugar level, respiratory distress syndrome, and type-2 diabetes to the mother. It creates a mandatory situation to identify the hyperglycaemia at least during the pregnancy weeks from 18 to 20. Further, a continuous monitoring of the level of glucose is necessary for the proper delivery. In this work, a method is introduced for glucose detection at 0.06 mg/mL, assisted by gold nanorod (GNR)-conjugated glucose oxidase (GOx) on interdigitated electrode sensor. In the absence of GNR, GOx shows the limit of glucose detection to be 0.25 mg/mL. Moreover, with GOx-GNR the reactions of all the glucose concentrations have recorded higher levels of the current from the baseline. With the specificity analysis, it was found that the glucose only reacts with GOx-GNR and discriminates other sugars efficiently. This method of detection is useful to diagnose and continuously monitor the glucose level during the pregnancy period.
This study aimed to identify the independent and combined effects of age, BMI at first prenatal visit and GWG on the risk of GDM. A retrospective cohort study of 1,951 pregnant women in Seremban district, Negeri Sembilan, Malaysia. GDM was defined as fasting plasma glucose (FPG) ≥5.6 mmol/l and/or 2-hour postprandial plasma glucose (2hPPG) ≥7.8 mmol/l. A higher percentage of women with GDM had 2 risk factors (29.0%) or >2 risk factors (8.6%) compared to non-GDM women (2 risk factors: 25.5%; >2 risk factors: 5.0%). In general, women with ≥2 risk factors were respectively 1.36-2.06 times more likely to have GDM compared to those without risk factors. Older maternal age and being overweight/obese were significantly associated with risk of GDM. Overweight/obese women with age ≥35 years had 2.45 times higher risk of GDM and having excessive GWG at second trimester further increased the risk of GDM. Age and BMI are independent risk factors for GDM but not GWG in the first and second trimester. The findings emphasize the need to focus on a healthy BMI before pregnancy and optimal GWG during pregnancy to improve pregnancy outcomes.
BACKGROUND: Septal hypertrophic cardiomyopathy (sHCM) is a characteristic anomaly of the infant of diabetic mother (IDM). Insulin-like growth factor-1 (IGF-1) has been identified as a mediator of tissue overgrowth and we have previously shown that maternal IGF-1 levels were significantly elevated among neonates with asymmetrical sHCM. IGF-1 does not cross the placenta; it exerts physiologic action through binding to the IGF-1 receptor (IGF-1R). Localisation and expression of IGF-1R in term diabetic pregnancies are largely unclear. We have studied IGF-1R in the placentae of diabetic and normal pregnancies and this receptor expression in association with neonates with sHCM.
METHODS: IGF-1R localization and expression in the placentae of six diabetic pregnancies associated with neonatal sHCM were compared with six each of randomly selected diabetic and normal pregnancies without neonatal sHCM by immunohistochemistry. The staining for IGF-1R in the deciduas, cytotrophoblasts, syncytiotrophoblasts and villous endothelium for these 18 samples were assessed and scored by two pathologists who were blinded to the respective diagnoses.
RESULTS: Placental IGF-1R staining was negative in the villous endothelium for all three groups. IGF-1R staining was present in deciduas, cytotrophoblasts and syncytiotrophoblasts but the staining was weaker in the entire group of infants with sHCM compared to those without sHCM.
CONCLUSIONS: IGF-1R is localized in all cell types of the placenta except in villous endothelium. Weaker placental IGF-1R staining in the placentae of diabetic pregnancies associated with sHCM suggests reduced expression of IGF-1R. This may be a down-regulatory response to elevated maternal IGF with neonatal sHCM outcome.